Effect of DHPR on Functional Properties, Energy, and Ca2+ Metabolism of m. soleus during Unloading

Dihydropyridine receptors (DHPR) participate in changes of the membrane potential during muscle unloading. We used nifedipine, a dihydropyridine derivative and Ca2+ antagonist, to study the role of L‑type Ca2+ channels (Cav1.1, DHPR) in regulation of energy and Ca2+ metabolism and impact on functional properties of m. soleus during unloading. Male rats were divided into 3 groups (n = 16 in each group): vivarium control with placebo (C), 3-day hindlimb suspension with placebo (HS), and 3-day hindlimb suspension with intraperitoneal administration of the nifedipine (N). It was found that nifedipine administration during hindlimb suspension produced the following effects: (1) it decreased the ATP accumulation; (2) prevented the reduction of the maximum force of a single contraction and the time of contraction, and (3) prevented the increase in the content of intramitochondrial and myoplasmic calcium. Thus, DHPR participates in energy and Ca2+ metabolism and affects the functional properties of muscles.